Malignant hypertension has usually been viewed in terms of severely elevated arterial pressure, renal failure and elevated plasma renin levels. Other factors, however, may play an important role as indicated by our recent observations in conscious dogs in which malignant hypertension could be produced consistently by constriction of both renal arteries. Two distinctly different forms of malignant hypertension sharing a common symptomotology were identified. One form was characterized by low cardiac output, the appearance of hemolysis in plasma and responsiveness to treatment with propranolol; the other was associated wth increased cardiac output, lack of hemolysis and was nonresponsive to treatment with propranolol. Further investigation of the mechanisms responsible for these different types of malignant hypertension should lay the groundwork for a final understanding of the factors involved in the genesis of renal hypertension. We propose to characterize the hemodynamic and humoral changes that occur in each type; the latter will include evaluation of the roles of the renin-angiotensin system, prostaglandins and the possibility that a presently unidentified humoral factor may contribute to fibrin deposition and development of vascular lesions.